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Figure 4 | Journal of Inflammation

Figure 4

From: Silencing collapsin response mediator protein-2 reprograms macrophage phenotype and improves infarct healing in experimental myocardial infarction model

Figure 4

CRMP2 was predominantly expressed in M1 but not M2 macrophages infiltrated in the wound of wildtype and ApoE −/− mice with MI. A & B. Representative confocal microscopy images showed the predominance of M1 (CD11b+, iNOS+) macrophages 3 days after MI in both wildtype and ApoE−/− mice with MI, and predominance of M2 (CD11b+, IGF-1+) macrophages in wildtype but predominance of M2 (CD11b+, IGF-1+) macrophages in ApoE−/− mice 10 days after MI. Scale bar indicates 50 μm. C. Quantitation of M1 (CD11b+, iNOS+) macrophages in the wound 3 and 10 days after MI. D. Quantitation of M2 (CD11b+, IGF-1+) macrophages in the wound 3 and 10 days after MI. E. Representative confocal microscopy images showed the expression of CRMP2 in the infiltrated macrophages 3 days after MI in ApoE−/− mice. Arrows indicated localization of CRMP2 in one pole outside of the nucleus. F. Representative confocal microscopy images showed the expression of CRMP2 in the infiltrated macrophages 3 days after MI in WT mice. G. Quantitation of CRMP2 positive macrophages in the wound 3 and 10 days after MI in WT and ApoE−/− mice. In all of the quantitative experiments, n = 4 mice per group and n = 4 high power fields (hpf). Data are mean ± SEM. *P < 0.05 compared to WT control.

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